Evidence map›Paper›PMID 40399501›Full record

ArticleScientific reports2025

Identification of CLEC10A as a human lectin for pancreatic ductal adenocarcinoma.

Shuntaro Tsukamoto, Hiroaki Tateno, Osamu Shimomura, Kana Yamamoto, Sayoko Saito, Jinko Murakami, Hiromitsu Nakahashi, Yoshihiro Miyazaki, Tsuyoshi Enomoto, Tatsuya Oda

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. GlycoChat Uncovers Glycan-Lectin Circuits in the Tumor Microenvironment of Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Shuntaro TsukamotoDepartment of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Hiroaki TatenoCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan. h-tateno@aist.go.jp.
Osamu ShimomuraDepartment of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Kana YamamotoCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan.
Sayoko SaitoCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan.
Jinko MurakamiCellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Japan.
Hiromitsu NakahashiDepartment of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Yoshihiro MiyazakiDepartment of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Tsuyoshi EnomotoDepartment of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Tatsuya OdaDepartment of Gastrointestinal and Hepato-Biliary-Pancreatic Surgery, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan. tatoda@md.tsukuba.ac.jp.

Funding

Japan Agency for Medical Research and Development 24jm0210100h0003Japan Science and Technology Agency JPMJTR20UDJapan Society for the Promotion of Science JP22K11444Japan Society for the Promotion of Science JP23K08186Japan Society for the Promotion of Science JP23K24172Japan Society for the Promotion of Science JP23K26872
6 · The paper itself

Abstract

The mechanism by which glycans in pancreatic ductal adenocarcinoma (PDAC) interact with human endogenous lectins in the tumor microenvironment remains largely unknown. This study aimed to identify endogenous lectins that recognize and bind to pancreatic ductal adenocarcinomas. The reactivity of 43 human endogenous lectins belonging to the Galectin, Siglec, and C-type lectin families in PDAC cell lines and clinical PDAC samples was analyzed using flow cytometry and immunostaining of tissues. C-type lectin domain family 10 member A (CLEC10A), a C-type lectin, was a candidate endogenous lectin with high reactivity in some pancreatic cancer cells. CLEC10A lectin bound in approximately 60% of 113 clinical pancreatic cancer tissue sections. Immunohistochemistry with anti-CLEC10A antibody showed that CLEC10A was mainly expressed in CD163-positive monocytic cells. Of the 57 patients (out of 113) who achieved R0 surgical resection at stage II/III, those with high CLEC10A expression on macrophages and CLEC10A ligand expression on PDAC cells had significantly shorter overall survival. CLEC10A is a human lectin receptor for pancreatic ductal adenocarcinoma. The coexistence of CLEC10A-expressing cells in pancreatic cancer tissues and CLEC10A ligands on pancreatic cancer cells indicates poor prognosis.

Indexed as

Carcinoma, Pancreatic DuctalLectins, C-TypePancreatic NeoplasmsAgedCell Line, TumorFemaleHumansMacrophagesMaleMiddle AgedPrognosisTumor MicroenvironmentCLEC10A protein, humanLectins, C-TypeCLEC10A proteinEndogenous lectinPancreatic cancerTumor microenvironment

Identifiers

PMID40399501
PMCPMC12095740

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.